Since Warren's group reported the existence of Helicobacter pylori [Former Name: Campylobacter pylori] in the human gastric mucosal (Warren J. R. et al., "Unidentified curved bacilli on gastric epithelium in active chronic gastritis", Lancet 1: 1273-1275 (1983)), numerous researches have been performed with regard to the biochemical properties thereof, in particular, the correlation between Helicobacter pylori and digestive diseases including gastric ulcer, duodenal ulcer or the like.
In view of the focus that Helicobacter pylori have been separated/detected at a high rate from the human gastric mucosa of the gastritis patients or the gastriculcer patients [e.g., there are reports that they were detected at a rate of 50.about.80% in the cases of chronic gastritis, superficial gastritis, atrophic gastritis, erosive gastritis or the like], and the symptom of these digestive diseases are alleviated with sterilization by administration of drugs, accordingly, the correlation between Helicobacter pylori and the digestive diseases were suggested.
Helicobacter pylori would not make an invasion upon mucosal cells, but stay on the epithelial mucosa surface and/or the intercellular space and grow (proliferate) thereat. Then, it is thought that PAS (Periodic Acid-Sciff) reaction positive layer in the gastric mucosa are thinned through growth of Helicobacter pylori, thereby, effects of mucin which protects mucosa are declined, and potency on defense factor of the gastric mucosa are also declined (T. Ito, "Recent findings on Helicobacter pylori", Medical Technology, 19 (10), pp. 892-893 (September 1991)).
Then, the mechanism was also reported that Helicobacter pylori arrive and stay in gastric mucosal epithelium, then ammonia were produced through degradation of urea in the stomach by urease from Helicobacter pylori, the ammonia so produced damage gastric mucosa and generate reverse diffusion of the hydrogen ion, and, tumors are thereby formed (Tsujii, M. et al., "Mechanism of gastric mucosal damage Induced by ammonia", Gastroenterology 107: pp. 1881-1888 (1992)).
In general, conventional diagnosis of Helicobacter pylori, which is correlative to the human digestive diseases, includes:
(1) Direct proof on presence of Helicobacter pylori in a part of mucosa [Smear, Tissue-Microscopy, Cultivation], PA1 (2) Detection utilizing character of Helicobacter pylori including urease activities, and PA1 (3) Seroimmunodiagnosis (T. Shirai et al., "Diagnosis on Presence of Campylobacter pylori", Saishin-Igaku, 44 (2), 284-288 (1989)).
Of the methods aforenoted, a method (cultivation method) for detecting Helicobacter pylori through micro-aerobic cultivation of biopsy sample on gastric mucosa is the most reliable and accurate method. But, this method usually needs about one hour for a cultivation to grow the bacteria, the longer time would therefore be necessary to obtain the test results.
Then, in consideration of urease productivity by Helicobacter pylori, a method for directly detecting urease in samples of gastric biopsy have also been utilized (T. Ito, "Special diagnosis for bacterial infection/4. Campylobacter pylori", Rinnshoui, 15 (supplement), pp. 367-369 (1989). However, since these are methods to test the biopsy samples with an endoscope, the methods need the skilled operation and the patients will suffer from the unbearable pain.
Further, since urea in the stomach are degraded into ammonia and .sup.14 CO.sub.2, there is a diagnosis including evaluation of such .sup.14 CO.sub.2 by a scintillation counter. But, this method also needs a skilled work to handle radioisotope.